The objectives of this study were: 1) to confirm superoxide anion radical (O ) formation, and 2) to monitor in real time the rate of O generation in an operating anion exchange membrane (AEM) fuel cell using in situ fluorescence spectroscopy. 1,3-Diphenlisobenzofuran (DPBF) was used as the fluorescent molecular probe owing to its selectivity and sensitivity toward O in alkaline media. The activation energy for the in situ generation of O during AEM fuel cell operation was estimated to be 18.3 kJ mol . The rate of in situ generation of O correlated well with the experimentally measured loss in AEM ion-exchange capacity and ionic conductivity attributable to oxidative degradation.

Podocytes are epithelial cells adhering glomerular capillaries, which regulate the integrity of glomerular filtration barrier. Irreversible podocyte injury induces glomerular inflammation and causes chronic renal diseases. Kcnq1ot1, a long non-coding RNA (lncRNA), participates in the pathogenesis of diabetic retinopathy and cardiomyopathy. However, its function in podocyte injury is elusive. Pyroptosis of murine podocyte MPC5 was triggered by sublytic complement C5b-9 (sC5b-9) for subsequent in vitro functional and mechanistic investigation. Gain/Loss-of-function analysis was conducted to examine the functional role of Kcnq1ot1 in podocyte pyroptosis. Meanwhile, the molecular mechanism of Kcnq1ot1's effect on podocyte injury was explored by identifying downstream molecules and their intermediate interactions. Kcnq1ot1 was upregulated in sC5b-9-induced podocytes, and silencing Kcnq1ot1 could inhibit sC5b-9's effect on podocyte pyroptosis. We also identified the interaction between Kcnq1ot1 and miR-486a-3p, through which Kcnq1ot1 mediated miR-486a-3p inhibition by sC5b-9. Furthermore, miR-486a-3p reduced the transcriptional activity of NLRP3, while the overexpression of NLRP3 enhanced sC5b-9's effect on podocyte pyroptosis through activating NLRP3 inflammasome. sC5b-9 induces pyroptosis in podocytes through modulating the Kcnq1ot1/miR-486a-3p/NLRP3 regulatory axis, and these uncovered key molecules might facilitate podocyte-targeted treatment for renal inflammatory diseases.

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Solar-driven desalination, which involves the conversion of solar energy to heat for freshwater generation, has been recognized as an attractive and sustainable desalination technology to alleviate freshwater shortage. In particular,...

V–Ce RFBs (∼100% CE and ∼70% EE over 100 cycles) using a CH3SO3H-based electrolyte and a AEM separator shows 30% higher capacity and 0.024% capacity fade/cycle vs. 5% capacity fade/cycle for H2SO4 supported V–Ce ED-RFBs.

Background: Long noncoding RNAs (lncRNAs) play critical and complex roles in regulating various biological processes of cancers. Our study aimed to investigate the involvement of lncRNA NCK1-AS1 in urinary bladder cancer (UBC). Methods: qRT-PCR was used to detect the expression of lncRNA NCK1-AS1 and miR-143 in UBC tissues and cells. The dual-luciferase reporter system assays were used to confirm the interaction between NCK1-AS1 and miR-143, and flow cytometry assays were applied to examine the behavioral changes in HT-1376 and HT-1197 cell lines. Results: It was observed that NCK1-AS1 was up-regulated, while miR-143 was downregulated in tumor tissues than in adjacent healthy tissues of urinary bladder cancer (UBC) patients. A 5-year survival analysis showed that the survival rate of patients with high NCK1-AS1 level or low miR-143 level in tumor tissues appears relatively low. Correlation analysis revealed a significant inverse correlation between NCK1-AS1 and miR-143 in tumor tissues. Over-expression NCK1-AS1 reduced the expression level of miR-143, while elevating the level of miR-143 failed to affect NCK1-AS1 expression. NCK1-AS1 over-expression led to promoted proliferation and increased percentage of CD133+ (stemness) cells. Conclusion: Therefore, NCK1-AS1 promotes cancer cell proliferation and increases cell stemness in UBC patients by down-regulating miR-143.

Redox-flow batteries (RFBs) enable large-scale energy storage at low cost due to the independent scaling of device power and energy, thereby unlocking energy arbitrage opportunities and providing a pathway to grid stability and resiliency. Herein we demonstrate an “electrode-decoupled” redox-flow battery (ED-RFB) with titanium and cerium elemental actives that has a clear pathway to achieve a levelized cost of storage (LCOS) of ca $0.025/kWh-cycle. A key enabling technology is our highly perm-selective modified poly(ether ketone)-based anion exchange membrane (AEM) that ensures long term separation of Ti and Ce species and enables capacity-fade-free cycling over 1300 hours of operation. Further, our Ti-Ce ED-RFB exhibits negligible capacity fade when the actives are charged to 90% state of charge (SOC), stored for close to 100-hours and then discharged, rendering it viable for long duration (load-following) grid-scale energy storage applications. Herein we introduce the Ti-Ce ED-RFB as a novel, low-cost long duration energy storage (LDES) system.

Background: Many studies have shown an elevated level of cholesterol in colon tumors as compared to normal tissue. Obesity and high low-density lipoprotein cholesterol (LDL-C) are known risk factors for colon cancer. However, the role of LDL-C in colon cancer patients with normal body mass index (BMI) remains elusive.Methods: Levels of serum cholesterol and oxysterols were quantified by ultra-performance liquid chromatography-tandem mass spectrometer (UPLC-MS/MS) from 129 individuals with normal BMI, including 32 with solitary polyp, 36 with multiple polyps, and 31 with adenocarcinoma as well as 32 healthy controls. In vitro, colon cancer cells were treated with LDL-C and assayed for chemokines via RNA-Seq and mitochondrial morphology via transmission electron microscopy and immunofluorescence. Additionally, correlation analysis was performed between LDL-C-induced chemokines and the overall survival of colon cancer patients from the Cancer Genome Atlas (TCGA), the Genotype-Tissue Expression (GTEx), and the Human Protein Atlas (HPA) database. Results:The serum cholesterol level was significantly higher in colon adenocarcinoma patients with normal BMI than that in healthy controls (P<0.001). LDL-C potentiated colon cancer cell invasion and resistance to glucose-deprivation in vitro via chemokine-mediated signaling, mainly upregulation of CC chemokine ligand (CCL) 5 and downregulation of CCL 11. By analyzing the RNA expression data of colorectal cancer from TCGA, GTEx, and HPA, we demonstrated that the CCL5 level in colorectal adenocarcinoma tissues was significantly increased relative to adjacent normal tissues (P=0.01) while the CCL11 level was decreased (P=0.01). Both increased CCL5 and decreased CCL11 showed a negative correlation with the 5-year overall survival in tumor node metastasis (TNM) stage II colon cancer patients (P=0.0032, 0.026 for CCL5 and CCL11, respectively). Conclusions:Our study supports the idea that LDL-C regulates the expression of CCL5 and CCL11 chemokines, which may have predictive values for survival in colon cancer patients with normal BMI, especially for patients in TNM stage II.